Perspective
Obesity and Cancer: Potential Mediation by Dysregulated
Dietary Phosphate
Ronald B. Brown






Citation: Brown, R.B. Obesity and
Cancer: Potential Mediation by
Dysregulated Dietary Phosphate.
Obesities 2022, 2, 64–75. https://
doi.org/10.3390/obesities2010007
Academic Editor: Carmine Finelli
Received: 27 December 2021
Accepted: 28 January 2022
Published: 2 February 2022
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Obesities 2022, 2, 64–75. https://doi.org/10.3390/obesities2010007
School of Public Health Sciences, University of Waterloo, Waterloo, ON N2L3G1, Canada;
r26brown@uwaterloo.ca
Abstract: Next to smoking, obesity is the second leading preventable risk factor for cancer, but in-
creasing rates of obesity and overweight are estimated to overtake smoking as the leading preventable
cancer risk factor. Few research studies have investigated the dysregulated endocrine metabolism of
dietary phosphate as a potential mediating factor in the association of obesity with cancer. Phosphate
toxicity, the accumulation of excess phosphate in the body from dysregulated phosphate metabolism,
is associated with tumorigenesis. High levels of hormones that regulate phosphate metabolism, such
as parathyroid hormone and fibroblast growth factor 23, are also associated with obesity, providing a
potential link between obesity and phosphate toxicity. Increased dietary intake of inorganic phosphate
is linked to excessive consumption of foods processed with phosphate additives, and consumption
of ultra-processed foods is associated with an increase in the incidence of obesity. Sugar-sweetened
beverages provide the single largest source of sugar and energy intake in the U.S. population, and
colas containing phosphoric acid are associated with tumorigenesis, suggesting another potential
connection between obesity and cancer. Furthermore, dietary phosphate is positively correlated with
increases in obesity, central obesity, and metabolic syndrome. The present perspective article proposes
that dysregulated dietary phosphate potentially mediates the association of obesity with cancer.
Keywords: obesity; cancer; tumorigenesis; dysregulated phosphate; phosphate toxicity; FGF23;
parathyroid hormone; vitamin D; phosphoric acid; ultra-processed food
1. Introduction
The World Health Organization (WHO) defined obesity as “abnormal or excessive fat
accumulation that may impair health,” caused by “an energy imbalance between calories
consumed and calories expended” [1]. Noting that “overweight and obesity, as well as their
related noncommunicable diseases, are largely preventable,“ WHO recommended reducing
obesity and overweight through supportive environments and communities that provide
easier access to regular physical activity, with more affordable and greater availability of
healthy food choices.
Next to smoking, obesity is the second leading preventable risk factor for cancer, but
increasing rates of obesity and overweight are estimated to overtake smoking as the leading
preventable cancer risk factor within the next two decades [2]. Yet, much of the population
remains unaware of the association of obesity with cancer [3]. Evidence is sufficiently
strong to link obesity with at least 13 sites of cancer: esophagus, stomach, colorectum, liver,
gallbladder, pancreas, breast, uterus, ovary, kidney, meninges, thyroid, and white blood
cells [4]. Paradoxically, a higher bodyweight has also been associated with reduced cancer
risk—an obesity paradox that some researchers suggest may be related to selection bias
from reliance on body mass index (BMI), which does not measure fat mass and fat-free
mass [5].
Hypotheses of the pathophysiological mechanisms linking obesity and cancer com-
monly investigate hormonal and enzyme dysregulation of glucose and lipid metabolism [6].
For example, obesity in humans is associated with higher levels of the hepatic protein kinase
https://www.mdpi.com/journal/obesities
Obesities 2022, 2 65

Cβ (PKCβ), which negatively regulates glycogenesis [7]. Dysregulated PKCβ is common

in many cancers and may be implicated in cancer development. Additionally, dysregulated
inositol synthesis in Drosophila melanogaster fed a high-sucrose diet is a potential model
for similar inositol abnormalities in human cancer and obesity [8]. However, few research
studies have investigated dysregulated endocrine metabolism of dietary phosphate as a
potential mediating factor in the association of obesity with cancer.
The present perspective article reviews epidemiologic and pathophysiologic rela-
tionships between obesity, unhealthy food choices associated with dysregulated dietary
phosphate, and tumorigenesis in obesity-related cancers. Articles from the research lit-
erature were selected and analyzed in this perspective paper using a grounded theory
method [9]. Keyword searches were conducted in Google, Google Scholar, PubMed, Scopus,
and other online sources. Comparative analyses of the literature findings were synthesized
into themes and formed into causative and associative relationships linking obesity, dys-
regulated phosphate metabolism, and cancer. All the findings and proposals in the present
perspective article are grounded in evidence, and offer the present author’s insights and
point of view.

2. Phosphate Metabolism
2.1. Phosphate Functions
The dietary mineral phosphorus, often found in chemical combination with oxygen
as phosphate (PO4 ), is an essential micronutrient with a dietary reference intake (DRI) of
700 mg/day for adults [10]. Phosphate performs a wide variety of functions in the human
body [11], as shown in Figure 1. Bones and teeth contain 85% of total body phosphate.
Inorganic phosphate (Pi) forms hydroxyapatite with calcium, which mineralizes the ex-
tracellular matrix of bone. The lipid bilayers of cell membranes contain phosphate, and
phosphate is a component in nucleic acids, deoxyribonucleic acid (DNA), and ribonucleic
acid (RNA). Energy is derived from the metabolism of adenosine triphosphate (ATP) and
adenosine diphosphate (ADP). Phosphate also acts as a urinary buffer, and many enzymatic
reactions involve inorganic phosphate.

Figure 1. Phosphate functions in the human body.

Obesities 2022, 2 66

2.2. Phosphate Regulation and Dysregulation

Serum Pi is regulated by a sensitive network of endocrine hormones that form a
bone–kidney–parathyroid–intestine axis, as shown in Table 1. Ref. [12]. Pi absorption in
the intestines occurs mainly through type II sodium-dependent phosphate cotransporters,
and intestinal absorption is regulated by bioactive vitamin D3 released by the kidneys,
1,25(OH)2 D3 , or calcitriol. The kidneys regulate serum Pi through reabsorption largely in
the renal proximal tubule. Fibroblast growth factor 23 (FGF23) released from osteocytes in
the bones, together with parathyroid hormone (PTH) from the parathyroid glands, reduce
high serum Pi levels by inhibiting kidney reabsorption of Pi and increasing Pi urinary
excretion [13]. PTH also increases the resorption of calcium from bone to maintain serum
calcium levels. Excess calcium phosphate formed in the blood serum from dysregulated
phosphate metabolism can lead to ectopic calcification deposited throughout the soft
tissue [14].

Table 1. Endocrine Regulation of Serum Pi through the Bone–Kidney–Parathyroid–Intestine Axis.

Bone Kidney Parathyroid Intestine

FGF23 inhibits serum Regulates serum Pi PTH increases serum
Pi absorption from
Pi reabsorption in reabsorption and Pi calcium through bone
dietary sources.
kidneys. urinary excretion. resorption.
Biosynthesis of
Type II
calcitriol from
Increases Pi urinary Increases Pi urinary sodium-dependent
vitamin D3 increases
excretion. excretion with FGF23. phosphate
Pi intestinal
cotransporters.
absorption.

3. Phosphate Toxicity and Tumorigenesis

Phosphate toxicity, the accumulation of excess phosphate in the body from dysregu-
lated phosphate metabolism, is associated with tumorigenesis [15]. Excessive cell growth
during tumor promotion and progression is stimulated by the uptake of excess phosphate
into cellular ribosomal RNA, and suppressed uptake of phosphorus within nuclear RNA
was shown to delay carcinogenesis in precancerous tissue [16]. High levels of phosphate
within the tumor microenvironment have been found to stimulate cell signaling in tu-
morigenesis [17] and tumor neovascularization [18]. Moreover, high phosphate levels
in patients with hyperphosphatemia are associated with chromosome instability and in-
creased parathyroid cell proliferation—further investigations of a direct effect of phosphate
on DNA damage are needed [19]. Additionally, high extracellular levels of Pi have been
linked to cancer progression through metastasis [20].
Cancer cells absorb and sequester large amounts of inorganic phosphate from the
tumor extracellular microenvironment through sodium-phosphate cotransporters, which
were overexpressed in cancer cells of the breast, lung, ovaries, and thyroid gland [21,22].
Levels of inorganic phosphate were up to twice as high in lung and colon tumor cells
compared to normal cells [23], and high dietary phosphate levels were found to increase
skin cancer growth in an animal model [24]. As well, lung tumorigenesis was stimulated
in mice fed high levels of dietary inorganic phosphate [17]. Cancer in humans was also
associated with higher serum phosphate levels in adults, with the exception of reproductive
cancers in females, which may be due to phosphate shifting into the reproductive tissue for
rapid growth [25,26].
More recently, H+ -dependent Pi transporters in breast cancer cells were found to trans-
port high concentrations of Pi at five-times the rate of sodium-phosphate cotransporters [27].
Patients with high levels of FGF23, which regulates Pi metabolism, had reduced overall sur-
vival compared to patients with low levels [28], and FGF23 levels were significantly higher
in patients with urothelial carcinoma of the bladder and upper urinary tract compared to
normal controls [29]. Additionally, compared to men with benign prostate hyperplasia,
men with prostate cancer had higher levels of PTH, which also regulates Pi metabolism [30].
Obesities 2022, 2 67

High serum PTH levels are associated with all-cause mortality in U.S. adults [31], and
patients with primary hyperparathyroidism had significantly higher risks of diagnosis with
cancers of the breast, skin, and kidney [32].

4. Phosphate Toxicity and Obesity

The same hormones that regulate phosphate metabolism are also associated with
obesity, providing a transitive link between obesity and phosphate toxicity. For example,
high serum FGF23 was associated with increased fat mass in a cohort of elderly white
people with normal renal function [33]. Participants in the study who had the highest
levels of FGF23 also had a significantly higher risk for overweight compared to individuals
with the lowest FGF23 levels. A 10% increase in FGF23 in the cohort was associated with a
3% increase in body weight and BMI and a 2% increase in waist circumference (WC) and
waist–hip ratio (WHR). Additionally, a 10% increase in FGF23 in males was associated with
a 4% increase in total body fat mass and trunk fat mass.
Hyperparathyroidism is commonly found in high-grade obesity, and higher serum
levels of PTH were found in 72% of bariatric patients with severe obesity who underwent
laparoscopic sleeve gastrectomy (LSG) [34]. Patients’ PTH levels dropped along with BMI
following surgery, likely related to a lower caloric density and volume of food intake
following LSG [35]. These findings imply that diet is an etiological factor in hyperparathy-
roidism related to obesity, which provides an additional transitive link between obesity
and phosphate toxicity from excessive dietary phosphate intake. Higher concentrations of
serum PTH were also positively associated with obesity in females with metabolic abnor-
malities, while levels of 25(OH)D3, which are converted to calcitriol to increase phosphate
absorption in the intestines, were inversely associated with obesity in males with metabolic
abnormalities [36].
Obesity is often associated with inadequate intake of micronutrients such as calcium,
magnesium, copper, iron, and zinc, but a recent analysis of the US National and Health Nu-
trition Examination Survey (NHANES) 2007–2014 found that phosphorus dietary intake
in adults, along with sodium, was positively associated with BMI [37]. Of relevance, type
II sodium-phosphate cotransporters (Na/Pi-2b) and type III inorganic phosphate trans-
porters (Pit-1 and Pit2) are found in the salivary glands, and obese and overweight children
were found to have significantly higher saliva levels of phosphate than normal-weight
children, despite having normal serum phosphate levels [38]. A plausible mechanism
accounting for higher saliva phosphate in obese and overweight children could be related
to increased salivary gland cotransport of phosphate from higher levels of ingested dietary
phosphate—more investigations are needed in this area.
Hypophosphatemia has also been linked to high BMI, but rather than resulting from
low dietary phosphate intake or phosphate losses in urine, low serum phosphate is most
frequently caused by a transcellular shift of internal phosphate [39]. Because dietary
carbohydrates require phosphorylation of glucose compounds during glycolysis, excessive
intake of carbohydrates releases increased levels of insulin which may cause phosphate to
shift from extracellular blood serum to liver and skeletal muscle cells during metabolism of a
heavy load of sugars [40]. Moreover, abdominal obesity is a part of metabolic syndrome [41],
and high serum levels of catecholamines in metabolic syndrome also increase metabolic
glycolysis of sugars, which further contributes to a phosphate transcellular shift that lowers
serum phosphate levels.
A paradoxical relationship also exists in the association of obesity with a lower risk
of breast cancer in premenopausal women compared to postmenopausal women [42].
The mid-luteal phase of the menstrual cycle is when the uterus undergoes growth [43],
and women self-reported consuming more animal-based foods during this phase [44].
Animal-based foods contain high levels of protein and phosphorus, which are needed to
support the monthly growth of the uterus. The need for more phosphorus during the
menstrual cycle could mitigate the risk of phosphate toxicity associated with heavy dietary
Obesities 2022, 2 68

phosphate intake in obese premenopausal women, which would lower the risk of breast
cancer compared to obese postmenopausal women.
Before closing this section on phosphate toxicity and obesity, it should be mentioned
that low levels of vitamin D are consistently linked with obesity and with cancer, but
researchers found that “the mediating role of vitamin D in the biological pathways linking
obesity and cancer is low” [45]. On the other hand, high serum Pi can signal endocrine-
controlled reductions in the renal biosynthesis of calcitriol (bioactive vitamin D), thus
lowering dietary phosphate intestinal absorption. In other words, low vitamin D appears to
be a consequence rather than a cause of dysregulated Pi metabolism in obesity and cancer.

5. Pi, Ultra-Processed Food, and Obesity

Increased dietary intake of inorganic phosphates is linked to excessive consumption
of processed foods, but the actual amount of phosphate intake from processed foods is
often unknown because food labels do not list the amount of inorganic phosphates in
food additives [46]. Inorganic phosphate is effectively absorbed in the body, and people
with a lower socioeconomic status (SES) consume the highest amount of processed and
convenience foods with added phosphate [47]. Of relevance, obesity in high-income
countries is more prevalent among people with a lower SES [48], inferring that a lower SES
mediates the association of greater Pi intake with high consumption of processed foods by
obese people.
Additionally, a recent prospective cohort study showed that consumption of ultra-
processed foods was associated with a 79% increase in the incidence of obesity measured
by BMI and a 30% increase in the incidence of abdominal obesity measured by WC [49].
Ultra-processed foods in the study included breads, snacks, desserts, frozen and ready-to-
eat meals, beverages, breakfast cereals, spreads, and sauces. Over a median of 5.6 years,
ultra-processed food consumption was associated with a 5% or higher risk of increasing
BMI, WC, and body fat percentage in the cohort. Another study found that a 10% increase
in ultra-processed food consumption was associated with a 10% and higher risk of breast
cancer and overall cancer [50]. Animal products with greater phosphorus absorption also
“contribute to the poor dietary habits linked with the rising rate of obesity in the USA”,
with every 0.5 mg/dL increase in serum Pi levels associated with a 2% increase in odds of
obesity [51].
Participants in a randomized controlled trial ate as much food as they wanted after
being assigned to either an unprocessed diet or an ultra-processed diet, served in meals
with equivalent amounts of nutrients and calories [52]. Over two weeks, the unprocessed
diet caused participants to eat less food, fewer calories, and lose a mean weight of 0.9 kg
compared to the ultra-processed diet which caused participants to eat more food, additional
calories, and gain a mean weight of 0.9 kg. Additional calories consumed in ultra-processed
foods were from carbohydrates and fats. Results reversed when the participants switched
diets. More studies are needed to measure the dietary intake of phosphorus from ultra-
processed diets compared to unprocessed diets.

6. Soft Drinks, Phosphoric Acid, and Obesity

Sugar-sweetened beverages provide the single largest source of sugar and energy
intake in the U.S. population [53] and also provide the largest source of sugar intake in the
Mexican population [54]. Obesity and weight gain associated with greater consumption
of sugar-sweetened beverages was found in systematic reviews of epidemiological and
experimental evidence in 2006 [55], in a majority of reviewed studies of children and
adolescents in 2015 [56], and in studies of adults and children in 2017 [57]. Another
systematic review and meta-analysis found that obesity was associated with artificially
sweetened as well as sugar-sweetened beverages [58].
In addition to an increased risk of obesity, a recent meta-analysis of prospective cohort
studies found that increased consumption of sugar-sweetened and artificially sweetened
beverages was associated with increased all-cause mortality [59]. A cohort study involving
Obesities 2022, 2 69

participants from the European Prospective Investigation into Cancer and Nutrition (EPIC)
found an association between a high risk of death from all causes and a high consumption
of total, artificially sweetened, and sugar-sweetened beverages [60].

Phosphoric Acid
Reports in clinical and experimental literature from 1970 to 1997 linked mineral
metabolism disorders and neoplasms with soft drinks such as colas that contain phosphoric
acid [61]. Consumption of cola soft drinks negatively affected biomarkers of bone, liver,
and kidney function in adult male rats [62]. A more recent study found that adult male
rats who consumed Pepsi Cola for three months had lower serum levels of vitamin D and
calcium but higher levels of phosphorus along with histopathological changes in the liver
and kidney tissue compared to a control group [63].
Consumption of phosphoric-acid-containing soft drinks was associated with hypocal-
cemia in children [64,65] and with elevated serum PTH, hypocalcemia, and hyperphos-
phaturia in postmenopausal women [66]. Hypocalcemia occurs when phosphate ions
from phosphoric acid consumed in cola react with serum calcium ions and precipitate into
calcium hydrogen phosphate—followed by a release of PTH that resorbs calcium from
bone to restore serum calcium levels [67]. Low bone mineral density in older women was
also associated with cola consumption but not with other carbonated beverages, which the
researchers attributed to mineral imbalances from the phosphoric acid in cola [68]. High
intake of sugar-sweetened beverages containing phosphoric acid was inversely associated
with bone health in a recent systematic review and meta-analysis [69], and cola intake was
inversely associated with bone mineral density in male adolescents and young adults from
the Korea National Health and Nutrition Examination Survey, 2008–2011 [70].

7. Soft Drinks and Cancer

Lab results of long-term carcinogenicity bioassays of Coca-Cola consumed by 1999 rats
showed an increase in bodyweight and increased incidence of malignant mammary tumors
and pancreatic adenomas, with insignificant increases in pancreatic islet cell carcinomas [71].
Consumption of sugary drinks, including 100% fruit juices, was associated with overall
cancer and breast cancer risk in a large prospective cohort study [72]. Researchers suggested
that the association of cancer with sugary drinks might be partially explained by the
relationship of consumption with overweight and obesity, which the researchers attempted
to adjust based on BMI. Sugar-sweetened beverage consumption among postmenopausal
women was also associated with an increased risk of type I endometrial cancer [73].
More recently, a higher risk of early-onset colorectal cancer among women was as-
sociated with higher sugar-sweetened beverage consumption in adolescence and adult-
hood [74]. A recent meta-analysis of observational studies also found that overall cancer
risk and mortality was associated with sugary drink consumption, especially for risk of
hepatocellular carcinoma, colorectal cancer, prostate cancer, and risk and mortality for
breast cancer [75]. Furthermore, another meta-analysis of observational studies found
that artificially sweetened soft drink consumption was associated with an increased risk
of liver cancer [76]. Consumption of a combination of sugar-sweetened and artificially
sweetened drinks and fruit juices was also associated with an increased risk of liver cancer
in a European cohort [77].
In response to the global obesity crisis, artificially sweetened beverages have been
proposed as an important part of a healthy diet—yet, evidence of their effectiveness to
prevent weight gain and long-term studies of their health effects are lacking for artificially
sweetened beverages, which also provide a low nutritional value and contain additive
ingredients [78]. Of relevance, artificially sweetened colas contain as much added phos-
phoric acid as sugar-sweetened colas, and the promotion of artificially sweetened colas
could potentially pose a risk of tumorigenesis and other adverse health effects associated
with dysregulated phosphate metabolism and phosphate toxicity. Investigations of phos-
phoric acid and dysregulated dietary phosphate in obesity and cancer should be given
Obesities 2022, 2 70

equal consideration to other dietary factors such as glucose and lipids contained in highly
processed foods.

8. Phosphate Additives and Obesity

In addition to soft drinks with added phosphoric acid, processed cheese contributes
the highest amount of phosphate additives in the American diet, according to an analysis of
NHANES 2015–2016 [79]. Other processed foods contributing high amounts of phosphate
include bakery products that utilize phosphate for leavening—pies and cakes, rolls and
buns, cookies and brownies, doughnuts, sweet rolls, pastries, and tortillas. The foods that
contribute the most total phosphate from a combination of natural and additive ingredients
are cheese, pizza, whole chicken pieces, reduced-fat milk, eggs and omelets, yeast breads,
and cold cuts and cured meats.
An analysis of a biracial cohort, Healthy Aging in Neighborhoods of Diversity across
the Life Span (HANDLS), found that cheese and yogurt consumption were associated with
an increased risk of central obesity [80]. Increased consumption of cheese and phospho-
rus intake were also positively correlated with increases in obesity (BMI), central obesity
(WC), and metabolic syndrome in a cross-sectional study of participants from NHANES
1999–2004 [81]. Furthermore, a dietary pattern with a low calcium: phosphorus ratio (low
calcium and high phosphorus) was also associated with increased obesity measured by
Waist to Height Ratio (WHtR) in a Brazilian population [82]. A Japanese study found that
patients with schizophrenia, “known to be prone to be overweight,” consumed more phos-
phorus than the general public, and phosphorus consumption was highest in patients with
higher BMIs [83]. The researchers suggested high phosphorus intake could be attributed to
patients who “often used fast food products.”
A study using a mouse model demonstrated that high amounts of dietary inorganic
phosphate altered cell signaling and increased tumorigenesis of the lungs [17]. Lead
investigator Myung-Haing Chou commented on the study:
“In the 1990s, phosphorus-containing food additives contributed an estimated
470 mg per day to the average daily adult diet,” Chou said. “However, phosphates
are currently being added much more frequently to a large number of processed
foods, including meats, cheeses, beverages, and bakery products. As a result,
depending on individual food choices, phosphorus intake could be increased by
as much as 1000 mg per day” [84].
If excessive consumption of ultra-processed food is an epidemiological determinant of
obesity and cancer, then modification of ultra-processed food intake and a return to dietary
patterns emphasizing whole, natural, unprocessed foods, is a viable strategy to prevent
these diseases. Nutritional epidemiologist Marian L. Neuhouser recently wrote:
“A shift towards healthy dietary patterns has the potential to curtail the current
unsustainable high level of obesity, cardiovascular disease, diabetes mellitus and
cancer in the United States and around the globe” [85].

9. Summary and Future Directions

The biological pathways linking obesity and cancer proposed in the present paper
are summarized in Figure 2—a directed acyclic graph (DAG) [86]. The dashed line in
the figure represents an associative relationship between obesity and tumorigenesis in
cancer involving suspected factors other than phosphate. This associative relationship
is potentially mediated by solid lines representing a pathway of causative links between
obesity and dysregulated dietary phosphate and between dysregulated dietary phosphate
and tumorigenesis. Mediation by these proposed causative relationships provides the basis
to generate testable hypotheses for further investigations of obesity and cancer.
Obesities 2022, 2 71

Figure 2. Obesity increases levels of dysregulated dietary phosphate, which mediates the association
between obesity and tumorigenesis.

Additionally, conditions comorbid with obesity could contribute to renal damage,

thereby increasing the risk of dysregulated phosphate, phosphate toxicity, and associated
tumorigenesis discussed in the present paper. Comorbid conditions such as atherogenic
dyslipidemia, hypertension, insulin resistance, and type 2 diabetes cause renal damage
in obesity through oxidative stress, inflammation, upregulation of the renin–angiotensin–
aldosterone system, increased activity of the sympathetic nervous system, and endothelial
dysfunction [87]. Future research should investigate the biological pathways between
obesity-related cancers and comorbid conditions involving impaired kidney function and
dysregulation of phosphate metabolism.
Finally, writing in the Lancet in 1996, Schipper et al. [88] proposed a new regulatory
model for cancer research. The researchers suggested that dysregulated metabolic path-
ways linked to the clinical course of cancer are reversible. Supporting evidence provided
by the researchers at the time included cancer cell genetic differentiation in treatment
for leukemia and recovery from gastric lymphoma related to the eradication of Helicobac-
ter pylori infection. More recently, supporting evidence linking dysregulated phosphate
metabolism and cancer appears highly concordant and coherent with the regulatory model.
The model can be used to guide future cancer research to test whether modification or
reversal of dysregulated phosphate metabolism through dietary interventions can alter
the clinical course of cancer. Restricted-phosphate diets are currently used to modify the
progression of chronic kidney disease [89], and similar diets should be tested for use in
patients with obesity-related cancers.

10. Conclusions
In conclusion, the evidence presented in this paper supports an endocrine pathway
in which dysregulated dietary phosphate potentially mediates the association of obesity
with cancer. Excessive consumption of ultra-processed foods and other foods high in
phosphate in obesity increase the intake of inorganic phosphate, phosphoric acid, and other
phosphate additives, leading to dysregulated dietary phosphate. In turn, dysregulated
dietary phosphate and phosphate toxicity are associated with tumorigenesis. Further
studies should investigate the involvement of dysregulated dietary phosphate and impaired
kidney function in obesity-related cancers.

Funding: This research received no external funding.

Institutional Review Board Statement: Not applicable.
Informed Consent Statement: Not applicable.
Obesities 2022, 2 72

Conflicts of Interest: The author declares no conflict of interest.

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